Page 76 - Organic Electronics in Sensors and Biotechnology

Or ganic Thin-Film Transistors for Inor ganic Substance Monitoring 53

Nitrogen oxide (NO) and nitrogen dioxide (NO ), usually termed
2
NO , enter the atmosphere from polluting sources as well as from
x
natural sources such as lightning and biological trials. NO gases of
x
anthropic origin mainly arise from the combustion of fossil fuels usu-
ally used to feed vehicle engine and from house heating. NO cause
x
several detrimental effects on the environment such as the photo-
chemical smog [a mixture of nitric acid, NO , inorganic and organic
x
nitrates, peroxyacetylnitrate (PAN), ozone, and other reactive oxygen
species], and acid rains. NO inhalation may result in several pulmo-
x
nary inflammations, and a constant exposure to 500 ppm of such
gases may cause death within 2 to 10 days. The allowed exposure
limit given by OSHA for NO is 25 ppm (averaged throughout an 8 h
exposure), while for NO a 5 ppm limit is set as a ceiling level. For
2
both gases, however, the alarm threshold is lower than 1 ppm, and
Italian legislation set their concentration limit at 100 and 200 ppb for
NO and NO ,respectively.
2
As previously discussed for CO, nitrogen oxide is also produced
in the human body (lung), and it is involved in several metabolic and
inflammatory processes. NO is synthesized endogenously by NO
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synthases (NOS). Three isoforms of NOS, which are products of
three separate genes, have been identified including neuronal (nNOS
or NOS I), endothelial (eNOS or NOS III), and iNOS (or NOS II).
These enzymes convert l-arginine to NO and l-citrulline in a reaction
requiring oxygen, NADPH, and many cofactors. 13
NO produced mainly by NOS II plays a key role in immunode-
fense and antiviral mechanisms of airway epithelium cells, and alter-
ation of its concentration in exhaled breath is a signal of a pathologi-
cal status. Indeed, a concentration increase of exhaled NO has been
demonstrated to be related to chronic inflammatory airway diseases
such as asthma, bronchiectasis, and other respiratory infections
including bacterial and viral illnesses. 14–16 Typically, NO concentra-
tion in exhaled breath of healthy subjects ranges from 5 to 10 ppb
while for asthmatic patients it falls in the range of 50 to 100 ppb. 17–18
On the other hand, a much too low NO concentration has been related
to the human immunodeficiency virus (HIV-1) and to cystic fibrosis,
thus suggesting the existence of viral mechanisms that suppress the
NO-related host defense. 14, 19, 20 More recently, the potential therapeu-
tic role of NO gas in cancer treatment has also been investigated. 21
Hence, NO can be considered as a signaling molecule of the
inflammatory response to viruses. Such an immunodefense action is
22
due to the NO activation of the guanylate cyclase to produce guano-
sine 3′,5′-cyclic monophosphate (cGMP) that acts as a second mes-
senger and relaxes the airway smooth muscles. Moreover, NO has an
antiviral effect 23, 24 since it is able to activate specific defensive enzymes
through protein modification processes such as nitration of tyrosine
and nitrosylation of thiols. 25, 26 Unlike NO, NO is not involved in any
2
physiological mechanism in the human body.